低氧训练对大鼠脑组织Ngb、HIF-1α、Bax和Bcl-2的影响

Effects of hypoxic training on brain tissues Ngb,HIF-1α,Bax and Bcl-2 of rats

探讨常压下模拟低氧(氧体积分数13.6%)训练对大鼠脑组织Ngb、HIF-1α、Bax和Bcl-2的影响,为运动和低氧适应提供理论参考。将50只9周龄雄性SD大鼠随机分为低住安静组、低住低练组、高住安静组、高住低练组和高住高练低练组,每组10只。训练组大鼠进行跑台训练,强度为常氧下35 m/min、低氧下30 m/min,持续运动1 h/d,5 d/周,持续4周。实验结束后,采用ELISΑ试剂盒分别检测大鼠脑组织Ngb、HIF-1α、Bax和Bcl-2水平,并计算Bax与Bcl-2的比值。结果发现:(1)与低住安静组比较,低住低练组HIF-1α、Bax和Bax/Bcl-2均升高(P<0.05或P<0.01);高住安静、高住低练和高住高练低练组的Ngb、HIF-1α、Bax和Bcl-2均升高(P<0.05或P<0.01)。(2)与低住低练组相比,高住安静、高住低练和高住高练低练组的HIF-1α和Bcl-2均升高(P<0.01);高住低练和高住高练低练组的Bax/Bcl-2降低(P<0.01);高住高练低练组的Ngb升高(P<0.01)。(3)与高住安静组相比,高住低练组和高住高练低练组的HIF-1α、Bcl-2均升高(P<0.05或P<0.01);高住高练低练组的Ngb升高(P<0.01),Bax/Bcl-2降低(P<0.05)。(4)与高住低练组相比,高住高练低练组Bcl-2升高(P<0.01)。(5)Ngb表达和HIF-1α表达呈正相关(r=0.563,P<0.01);Ngb表达与Bax/Bcl-2变化呈正相关(r=0.486,P<0.01);HIF-1α表达与Bax/Bcl-2变化呈正相关(r=0.353,P<0.05)。结果表明:单纯训练刺激会引起大鼠脑组织HIF-1α升高,单纯低氧刺激会引起大鼠脑组织Ngb和HIF-1α升高,当训练和低氧这两种因素相互结合时,Ngb和HIF-1α的升高更明显。高住高练低练对大鼠脑组织Bcl-2的影响要大于高住低练。Ngb和HIF-1α的升高,使Bax/Bcl-2向着有利于神经元存活的方向发展,提示Ngb和HIF-1α参与了中枢神经系统的缺氧耐受和自我保护。

The authors probed into the effects of hypoxic（13.6% oxygen content） training simulated under a normal pressure on brain tissues Ngb,HIF-1α,Bax and Bcl-2 of rats,so as to provide a theoretical reference for exercising and hypoxic adaptation.The authors divided 50 9 weeks old male SD rats randomly into a living low calm group,a living low training low group,a living high calm group,a living high training low group and a living high training high and low group;each group contained 10 rats.The rats in training groups were trained on a treadmill for 4 weeks at an intensity of 35m/min under a normal oxygen condition or 30m/min under a hypoxic condition,1h/d（continuous exercising）,5d/week.After the experiment was finished,an ELISA kit was used to respectively measure the levels of brain tissues Ngb,HIF-1α,Bax and Bcl-2 of the rats,and the ratio of Bax to Bcl-2 was calculated.The authors revealed the following findings： 1） as compared with living low calm group,the HIF-1α,Bax and Bax/Bcl-2 of the rats in living low training low group increased（P〈0.05 or P〈0.01）;the Ngb,HIF-1α,Bax and Bcl-2 of the rats in living high calm group,living high training low group and living high training and high and low group in-creased（P〈0.05 or P〈0.01）;2） as compared with living high calm group,the HIF-1α and Bcl-2 of the rats in living high calm group,living high training low group and living high training and high and low group increased（P〈0.01）;the Bax/Bcl-2 of the rats in living high training low group and living high training and high and low graoup de-creased（P〈0.01）;the Ngb of the rats in living high training and high and low group increased（P〈0.01）;3） as com-pared with living high calm group,the HIF-1α and Bcl-2 of the rats in living high training low group and living high training and high and low group increased（P〈0.05 or P〈0.01）;the Ngb of the rats in living high training and high and group increased（P〈0.01）,while their Bax/Bcl-2 decreased（P〈0.05）;4） as compared with living high training low group,the Bcl-2 of the rats in living high training and high and low group increased（P〈0.01）;5） Ngb expres-sion and HIF-1α expression showed a positive correlation（r=0.563,P〈0.01）;Ngb expression and Bax/Bcl-2 varia-tion showed a positive correlation（r=0.486,P〈0.01）;HIF-1α expression and Bax/Bcl-2 variation showed a positive correlation（r=0.353,P〈0.05）.The findings indicated the followings： training stimulation alone would cause the in-crease of brain tissue HIF-1 of rats;hypoxic stimulation alone would cause the increase of brain tissues Ngb and HIF-1α of rats;when such two factors as training and hypoxia were mutually combined,the increase of Ngb and HIF-1α would be more significant;the effects of living high training high and low on brain tissue Bcl-2 of rats were more significant than the effects of living high training low;the increase of Ngb and HIF-1α enabled Bax/Bcl-2 to develop in the direction favorable for neuron survival,which suggested that Ngb and HIF-1α had participated in the hypoxic tolerance and self protection of the central nervous system.